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Virus unmasked

By Philip Cohen in San Francisco

MAJOR steps towards understanding how the dangerous hepatitis C virus copies
itself and outwits medical treatment have been made in two new studies.

More than 150 million people worldwide have been infected by HCV. More than
three-quarters of them develop a chronic liver infection. But the virus is very
reluctant to replicate in the lab. So Ralf Bartenschlager of the University of
Mainz in Germany and his colleagues tried a new tactic. They genetically
engineered HCV DNA to include an antibiotic resistance gene, then introduced the
engineered virus into cells.

By using the antibiotic, the team could kill off cells the virus failed to
invade, and select only those in which the virus replicated. As expected, the
virus rarely infected cells. But when it did, it replicated efficiently (
Science, vol 285, p 110). “With these cells in hand, there is a lot we can
do,” says Bartenschlager. The system could be used to test how well different
drugs interrupt replication of the virus.

Interferon is the standard treatment for HCV. It switches on a protein called
PKR that shuts down production of proteins and viruses in infected cells. But
this drug works in less than half of patients. In Science(vol 285, p
107), a team led by Michael Lai of the University of Southern California in Los
Angeles explains why, showing that a common form of HCV makes a protein called
E2 that can bind to PKR and slash its activity by more than 90 per cent. Lai
says the discovery could lead to new drugs that treat hepatitis more
effectively.